PATH

Question 1

LIST BENIGN OSTEOGENIC TUMOURS

Answer 1

osteoid osteoma
osteoblastoma
osteoma

Question 2

LIST MALIGNANT CARTILAGE

Answer 2

Chondrosarcoma

Question 3

LIST MALIGNANT OSTEOGENIC

Answer 3

osteosarcoma

Question 4

AVASCULAR NECROSIS

Answer 4

infection of the bone and marrow due to loss of blood supply
AETIOLOGY: mechanical injury to vessels, thromboembolism, external pressures on vessels

may not be immediately visible on XRAY
legg-calve-perthes disease = children

Question 5

BONE TURNOVER - systemic

Answer 5

growth H and PTH work on chondrocytes to maintain proliferation and induce hypertrophy at growth plates
sex steroids increase bone growth by allowing OPG to outweigh RANK-L

Question 6

HYPERPARATHYROIDISM

Answer 6

caused by increase in PTH secretion from the pituitary gland
can be primary, secondary or tertiary
leads to increase in bone absorption - decreased bone mass etc

Question 7

RICKETS AND OSTEOMALACIA

Answer 7

manifestations of vit D deficiency
rickets: children, interfering with the deposition of bone in growth plates
osteomalacia: adults. bone formed in remodelling is undermineralised
skeletal pain and abnormalities - bowleggedness etc

Question 8

SKELETAL CHANGES IN RENAL OSTEODYSTROPHY
conditions + turnover

Answer 8

osteoporosis, osteomalacia, secondary hyperparathyroidism, stunted growth

can have high, low or mixed turnovers
secondary to chronic kidney disease

Question 9

LIST BENIGN CARTILAGINOUS TUMOURS

Answer 9

osteochondroma
enchondroma
juxtacortical chondroma

Question 10

BONE TURNOVER - local

Answer 10

osteoblasts produce RANK-L and MCS-F - osteoclast progenitors become osteoclasts
- FOCUS ON REMODELLING

osteoblasts produce OPG [Osteoprotegrin] - inhibiting osteoclast differentiation
- FOCUS ON BUILDING!

Question 11

LIST OTHER MALIGNANT TUMOURS

Answer 11

ewing sarcoma
multiple myeloma
metastatic tumours

Question 12

OSTEOGENESIS IMPERFECTA

Answer 12

autosomal dominant disease
Type 1 collagen synthesis defect - little bones that are easy to fracture
brittle bone disease

Question 13

SUMMARISE FRACTURE HEALING [w2+]

Answer 13

soft tissue callus becomes bony callus
- reparative phase.
woven bone is deposited; potential cartilage formation and endochondral ossification
excess of fibrous tissue, cartilage and woven bone
- remodelling phase
maturation of callus
weight bearing absorbs non-stressed bone

Question 14

PAGETS DISEASE

Answer 14

abnormal and excessive bone remodelling that creates unsound bone
presenting in late adulthood.
most commonly axial skeleton and femur.
has three phases: lytic, mixed and sclerotic
no early signs

Question 15

OSTEOPENIA / OSTEOPOROSIS

Answer 15

decreased bone mass. osteopenia advances into osteoporosis
primary cause is unclear
no clinical manifestations until break on minimal trauma

prominent in elderly women, endocrine / GIT disorders, drugs, 0 gravity etc

Question 16

OSTEOMYELITIS

Answer 16

inflammation of bone marrow secondary to infection
different spread/areas based on age
- children: haematogenous metaphysis
- adults: implantation epiphysis/ subchondral
- neonates epiphysis and metaphysis

Question 17

WHAT IS ACHONDROPLASIA

Answer 17

autosomal dominant disease
overly inhibited growth at plates due to FGFR3 mutation
little people!!

Question 18

SUMMARISE FRACTURE HEALING [week1]

Answer 18

haematoma forms -> soft tissue callus
influx of inflammatory cells and fibroblasts into the mesh that clots blood.
release of growth factors by platelets and inflam cells
activation of osteoprogenitor cells. stimulation of osteoblast and osteoclast